Hearts excised from 400-500g male wistar rats were perfused in the working mode. The mean aortic pressure was 80 mmHg and the mean left atrial pressure or preload at 10 cm H2O. The perfusion medium comprised 10 Mm glucose (no insulin), 117 Mm NaCl, 5.9 Mm KCl, 25 Mm NaHCO3, 1.2 Mm NaH2PO4, 1.12 Mm CaCl2 (free Ca2+=1.07 Mm), 0.512 Mm MgCl2 (free Mg2+=0.5mM) pH7.4 at 38 degrees C, with and without 75 Mm ethanol. The perfusate was vigorously bubbled with 95% O2, 5% CO2, and was not recirculated in the heart. In the presence of 75 Mm ethanol, the cardiac output fell by 40%, aortic flow by 60%, oxygen consumption by 17% and the power output by 42%. Mean values for cardiac output, aortic flow, oxygen consumption and power output in control hearts were 38.6 ml/min, 19.7 ml/min, 9.83 umol O2/min/g left ventricle and 415 mjoules/min/g left ventricle respectively (n=7). The presence of ethanol in the perfusion medium resulted in a 23% reduction in heart mitochondria (NAD/NADH ratio decreased from 3.95 to 3.04), a change that was similar in magnitude and direction to the decrease in the oxygen consumption (17%). The most important finding of this study on the acute effects of ethanol on heart function, was that the magnitude of the fall in oxygen consumption in the presence of 75mM ethanol was only 40% of the decrease in power output indicating a mismatch between supply and demand. This result may have potential clinical implications.